Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/11966
CCAAT/enhancer binding protein beta deficiency provides cerebral protection following excitotoxic injury.
J Cell Sci. 2008; 121(Pt 8):1224-34
The CCAAT/enhancer-binding protein beta (C/EBPbeta, also known as CEBPB) was first identified as a regulator of differentiation and inflammatory processes in adipose tissue and liver. Although C/EBPbeta was initially implicated in synaptic plasticity, its function in the brain remains largely unknown. We have previously shown that C/EBPbeta regulates the expression of genes involved in inflammatory processes and brain injury. Here, we have demonstrated that the expression of C/EBPbeta is notably increased in the hippocampus in a murine model of excitotoxicity. Mice lacking C/EBPbeta showed a reduced inflammatory response after kainic acid injection, and exhibited a dramatic reduction in pyramidal cell loss in the CA1 and CA3 subfields of the hippocampus. These data reveal an essential function for C/EBPbeta in the pathways leading to excitotoxicity-mediated damage and suggest that inhibitors of this transcription factor should be evaluated as possible neuroprotective therapeutic agents.
Animals | Brain Injuries | CCAAT-Enhancer-Binding Protein-beta | Cells, Cultured | Hippocampus | Immunohistochemistry | Kainic Acid | Male | Mice | Rats